The specific goal of this research project is to test the hypothesis that the Medtronic InterStim II Neurostimulator coupled with 3889 SNS Leads can be used for subcutaneous nerve stimulation (SCNS) to achieve rhythm and rate control of atrial fibrillation (AF) in a canine model. If the canine studies are successful, we will perform pilot clinical trials to facilitate rate control in patients with AF and rapid ventricular responses. The ultimate goal is to motivate Medtronic Inc. to perform additional clinical studies for FDA approval of SCNS as a labeled indication for managing AF. The study is responsive to the RFA-RM-16-027 because it will utilize existing market-approved technology for new market indications. AF is the most common cardiac arrhythmias in developed countries, and is associated with significantly increased mortality and morbidity. Drugs used for rate and rhythm control of AF are not uniformly successful and may be associated with significant side effects. Catheter ablation of the atrioventricular (AV) node is an option for rate control in patients with drug-refractory AF and rapid ventricular responses. However, AV node ablation makes the patient pacemaker dependent. It is highly desirable to develop an alternative method for AF control without the use drugs or ablation procedures. Histological studies showed that skin is well innervated by sympathetic nerves. In dogs, the postganglionic sympathetic nerve fibers of neck and thorax come primarily from the stellate ganglion (SG). Our preliminary studies showed that subcutaneous nerve stimulation (SCNS) from different sites in the thorax can damage SG and reduce SG nerve activity (SGNA). These findings suggest an exciting possibility that electrical stimulation of the skin may reduce SGNA to provide both rate and rhythm control of AF. Medtronic Inc. has a number of neurostimulators approved by FDA for pain and urinary control. The purpose of the present study was to test the hypothesis that the InterStim II Neurostimulator and the 3889 SNS Leads can be used effectively for SCNS and control AF. If the results are promising, it is possible to motivate Medtronic to sponsor pilot clinical studies and translate these findings to human patients. We propose the following specific aims: Specific Aim 1: To perform SCNS at various outputs to test the hypotheses that the magnitudes of output is important in determining the effects of neuromodulation. Specifically, high output stimulation causes SG damage and reduce sympathetic tone while very low output SCNS can cause SG and cardiac nerve sprouting, thus increasing the sympathetic tone. Specific Aim 2: To test the hypothesis that SCNS at high output is effective in rate and rhythm control of AF while at very low output is proarrhythmic. If SG damage underlies the mechanisms of the antiarrhythmic effects of SCNS, then it follows that high output SCNS is both necessary and sufficient to generate antiarrhythmic effects. On the other hand, if very low output SCNS causes nerve sprouting and increases sympathetic tone, then low output stimulation should be proarrhythmic. We will use a canine model of paroxysmal and persistent AF to test these hypotheses.